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Yr 2 - Pharmacology > Treatment of CNS disorders > Flashcards

Treatment of CNS disorders Flashcards

1
Q

Which channels are opened when a neurotransmitter binds on the post synaptic membrane in excitatory neurones?

And what does this cause?

A

Na in K out= depolarisation of the membrane

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2
Q

Which channels are opened when a neurotransmitter binds on the post synaptic membrane in inhibitory neurones?

And what does this cause?

A

Cl in = hyper polarisation of the membrane

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3
Q

Give an example of a glial cell:

A

Astrocyte

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4
Q

How do glial cells modulate the shape of post-synaptic response?

A

Remove the neurotransmitter from the synaptic cleft

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5
Q

Compare the following features of the Nervous system and Endocrine:

Mediator molecules

Cells affected

Time of onset of action

Duration of action

A
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6
Q

What criteria must a chemical meet before it can be called a neurotransmitter? (3)

A

Must be synthesised and stored within a pre-synaptic neurone (neurone must contain synthesising enzyme)

Stimulation causes release of the chemical from the nerve terminal (depolarisation)

Must cause the same effect as nerve stimulation on the postsynaptic neurone when applied directly onto the neurone

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7
Q

How many neuroactive substances can be found in the CNS?

A

Approx. 40

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8
Q

What type of channels are inotropic receptors?

A

Ligand-gated ion channels

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9
Q

What type of channels are metabotropic receptors?

A

GPCRs

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10
Q

List the (7) major CNS transmitters:

A

Glutamate

GABA

Acetylcholine

Monoamines (Noradrenaline, Dopamine & Serotonin)

Histamine

Opioids

Nitric Oxide (synthesised on demand & easily crosses the phospholipid bilayer -> its release is not Ca dependant but its synthesis is!)

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11
Q

What causes a neurotransmitter to have a dual response?

A

It acts on both Ionotropic receptors (faster inital response) AND metabotropic receptors (slower inital response because it takes a while for the second messenger to be synthesised)

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12
Q

What do neuromodulators do?

A

They alter the strength of response

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13
Q

What do neurotrophic factors do?

A

Influences neuronal differentiation and proliferation

(most do this by acting on Tyrosine kinase receptors)

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14
Q

What are the (4) different targets for drug action?

A

Ion channels

Receptors

Enzymes

Transporter proteins

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15
Q

Name an excitatory neurotransmitter in the CNS:

A

Glutamate

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16
Q

Name an inhibitory neurotransmitter in the CNS:

A

GABA

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17
Q

Which drug targets transmitter synthesis in the CNS?And what is the clinical application of this drug?

A

L- Dopa

Parkinson’s disease

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18
Q

Which drug targets transmitter storage in the CNS?And what is the clinical application of this drug?

A

Reserpine

Hypertension

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19
Q

Which 2 drugs targets transmitter release in the CNS? And what is the clinical application of this drug?

A

Amphetamine

Na & Ca channel blockers

Attention Deficit Hyperactivitiy disorder (ADHD)

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20
Q

Name 2 receptor agonists in the CNS?

And what is the clinical application of this drug?

A

Morphine (analgesia)

Buspirone (Anxiety)

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21
Q

Name 2 receptor antagonists in the CNS?

And what is the clinical application of this drug?

A

Cloazapine (antipsycotic)

Memantine (alzheimers)

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22
Q

Which 2 drug target reuptake in the CNS?

And what is the clinical application of this drug?

A

Cocaine (stimulant)

Fluoxetine (depression)

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23
Q

Which 2 drugs target degradation in the CNS?

And what is the clinical application of this drug?

A

Moclobemide (depression)

Donepezil (alzheimers)

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24
Q

Which drug targets intracellular signalling in the CNS?And what is the clinical application of this drug?

A

Lithium

Bipolar disorder

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25
Q

Which drug targets nerve growth in the CNS?

And what is the clinical application of this drug?

A

Myotrophin

Motor neurone disease

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26
Q

Why is it not a good idea to completely ‘knock out’ a neurotransmitter?

Give an example:

A

Bad side effects -> widely spread

e.g. Completely knock out glutamate = coma

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27
Q

Name 2 examples of drugs that target Glutamate:

(include their clinical use)

A

Ketamine = NMDA channel blocker (one of the inotropic receptors of Glutamate) => dissociative anaesthetic

Memantine = NMDA receptor antagonist => cognitive enhancer (in alzheimers)

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28
Q

What may drugs that target glutamate be used to treat? (4)

A

Learning and memory

Schizophrenia

Mood disorders

Excitotoxicity

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29
Q

Name the key 2 examples of drugs that target GABA: What are their clinical uses?

A

Benzodiazepines: Sedative hypnotic

Barbituates: Sedative hypnotic

Others:

Vigabatrine: GABA transaminase inhibitor = anti-epileptic

Alphaxalone: steroid general anaesthetic

Baclophen: GABA B angonist = spascticity

GHB: drug of abuse

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30
Q

In which (3) illnesses are GABA B recreptors for GABA targetted?

A

Epilepsy

Anaesthesia

Cerebral Palsy

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31
Q

Name the 3 main types of monoamine neurotransmitter:

A

Dopamine

Serotonin

Noradrenaline

N.b. these are difficult to target individually = aggressive & irritable moods if more than 1 disrupted by drug

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32
Q

Treatments for which 5 disorders target dopamine?

A

Parkinson’s disease

Schizophrenia

Drug abuse and addiction

ADHD (attention deficit hyperactivity disorder)

Depression

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33
Q

If drugs such as L-DOPA are given in the wrong situation what can it induce?

A

Schizophrenia like symptoms & hallucination

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34
Q

What does L-DOPA target? And what is its clinical use?

A

Bypasses the rate limiting synthetic enzyme for Dopamine

Parkinson’s disease

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35
Q

What does Haloperidol target?

And what is its clinical use?

A

D2 receptor antagonist

Anti-psychotic

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36
Q

What does Domperidone target?

And what is its clinical use?

A

D2 receptor antagonist

Anti-emetic

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37
Q

What does Selegeline target?

And what is its clinical use?

A

Monoamine oxidase - B inhibitor (MAO-B)

Neurodegeneration

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38
Q

What does Amantadine target?

And what is its clinical use?

A

Dopamine releasing agent

Parkinson’s disease

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39
Q

What does Amphetamine (methylphenidate) target?

And what is its clinical use?

A

Re-uptake inhibitor

Attention deficit hyperactivity disorder (ADHD)

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40
Q

What does Buproprion target? And what is its clinical use?

A

Dopamine/noradrenaline reuptake inhibitor

Anti-craving

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41
Q

What is Pramipexole?

A

Dopamine partial agonist

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42
Q

Treatments for which (7) disorders target noradrenaline?

A

Cognition

Depression

Anxiety

Pain

Addiction

Obesity

ADHD

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43
Q

What are the main functional effects of noradrenaline?

A

Attention

Cognition

Sensory

Homeostasis

Sympathetic output

Sleep-wake cycle

Motivation

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44
Q

What does Amitriptyline target? And what is its clinical use?

A

Serotonin and Noradrenaline reuptake inhibition

Pain & antidepressant

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45
Q

What does Reboxetine target?

And what is its clinical use?

A

Noradrenaline reuptake inhibition

Antidepressant

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46
Q

What does Sibutramine target? And what is its clinical use?

A

Serotonin & Noradrenaline reuptake inhibition

Anti-obesity

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47
Q

What does Mirtazapine target?

And what is its clinical use?

A

Alpha 2 adrenoreceptor and serotonin receptor antagonist

Antidepressant

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48
Q

What does Atomoxetine target?

And what is its clinical use?

A

Noradrenaline reuptake inhibiton

ADHD

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49
Q

What does clonidine target?

And what is its 2 clinical uses?

A

Alpha 2 adrenoreceptor agonist

Anti-hypertensive & epidural anaesthetic

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50
Q

What does Lofexine target?

And what is its clinical use?

A

Alpha 2 adrenoreceptor antagonist Opiate withdrawal

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51
Q

What are the (8) functional effects of serotonin in the CNS?

A

Motor control

Behavioural control

Mood and emotion

Sensory function

Homeostasis

Sleep-wake cycle

Appetite

Vomitting

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52
Q

Which (6) diseases are drugs that target serotonin used to treat?

A

Depression

Anxiety

Pain

Schizophrenia

Migraine

Emesis (vomitting)

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53
Q

What does Clomipramine target?

And what are its 2 clinical uses?

A

Serotonin reuptake inhibitor

Depression & OCD

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54
Q

What does Amitriptyline target?

And what are its 2 clinical uses?

A

Serotonin & noradrenaline reuptake inhibitor

Depression & OCD

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55
Q

What does Sibutramine target?

And what is its clinical use?

A

Serotonin and noradrenaline reuptake inhibitor

Anti-obesity

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56
Q

What does Fluoxetine target?

And what are its two clinical uses?

A

Serotonin reuptake inhibitor

Depression & eating disorders

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57
Q

What does Nefazedone target?

A

Serotonin reuptake inhibitor & Serotonin 2 receptor antagonist

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58
Q

What does Risperidone target?

And what is its clinical use?

A

Serotonin 2 receptor & dopamine 2 receptor antagonists

A-typical anti-psychotic

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59
Q

What does buspirone target?

A

Serotonin 1A receptor partial agonist

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60
Q

What does Sumatriptan target?

A

Serotonin 1B/D receptor agonist

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61
Q

What does Ondasetron target?

And what is its clinical use?

A

Serotonin 3 receptor antagonist

Anti-emetic

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62
Q

What does serotonin 1A receptor effect?

A

Mood

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63
Q

What does serotonin 1B/D receptor effect?

A

Vasculature

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64
Q

What does serotonin 2A/C recptor effect?

A

Behaviour

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65
Q

Why are more isoform selective drugs better?

A

They have fewer unwanted side-effects

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66
Q

What are anticholinergics used in clinically?

A

Parkinson’s disease

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67
Q

What are acetylcholinesterase (ACHE) inhibitors used for clinically?

A

Alzheimers disease

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68
Q

What is Acetylchonine involved in in the CNS?

A

Cognition

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69
Q

What are the 2 clinical uses of H1 antagonists in the CNS?

give an example

A

Sedation and Antiemetic(Possible role in cognition and mood)

Modafinil

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70
Q

Give an example of a purine (ATP) receptor anatagonist:

A

Caffiene

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71
Q

Which 3 things are purine (ATP) receptor agonists used for clinically?

A

Potentially:

Sedative

Anti-convulsants

Neuroprotection

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72
Q

What are purines (ATP) important for in the CNS?

A

Neuronal damage to the surrounding tissues when released (can even be neurotoxic)

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73
Q

What is the normal role of cannabinoids in the CNS?

A

Feedback loop for neurotransmitter release in synapses

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74
Q

What are the two types of stroke and which % of strokes do they account for?

How is each treated?

How do we determine which type it is?

A

Ischaemic (thrombosis) = 85%

Treatment: Anticoagulants/thrombolytics Haemorrhagic (rupture) = 15%

Treatment: Surgery to clock haemorrhage CT scan

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75
Q

Which artery is the most frequently effected in a stroke?

A

Middle Cerebral artery (a continuation of the internal carotid artery)

N.B. it is the only artery supplying this area of the brain -> blockage = death

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76
Q

What does an old infarction look like?

A

Significant tissue loss on the affected side & cystic change

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77
Q

Why is a lack of blood supply to the brain so detrimental?

A

The blood supplies O2 and Glucose to the brain tissue = metabolism -> the brain does not store glucose!

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78
Q

What is the treatment for a stroke?

A

Fibrinolytics within 3 hours = tissue plasminogen activators = improve blood flow and reduce further damage :( makes worse if due to haemorrhage!

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79
Q

In which 3 ways can we prevent strokes?

A
  • controlling blood pressure
  • Aspirin
  • Prevent atherosclerosis (low cholestrol diet & excersize)
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80
Q

What is a motorneurone disease?

A

A chronic progressive degeneration of lower and upper motor neurones in the spinal cord, somatic motor nuclei of the cranial nerves & within the cortex (N.B. does not involve the sensory neurones)

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81
Q

When do motor neurone diseases onset?

A

Middle life

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82
Q

What are the (7) signs of a lower motor neurone lesion?

A

Muscle wasting

Hypotonia

Reflex Loss

Fasciculation

Contractures of muscle (random contraction of skeletal muscle = spasm/twitch)

Muscle weakness

‘Trophic’ changes in skin and nail

83
Q

What is Amyotrophic lateral sclerosis?

A

Disease of lateral corticospinal tracts = atrophy of muscle

Clinical picture:

progressive spastic tetraparesis or paraparesis with added lower motor neurone signs and fasciulation

Atrophy of the nerve roots & loss of characterisitic large motor neurones (anterior horn cells)

84
Q

Name a disease modifying treatment of motor neurone diesease:

A

Riluzole = inhibits both the release and postsynaptic action of glutamate = protects from exocytotoxicity

85
Q

What is the extrapyrimidal system involved in (4)?

A

Crude movements

Integrates motor and sensory impulses

Co-ordinatwa muscle tone reflexes and movements

Facilitate and restrain anterior horn neurone activity

86
Q

What 4 things do disorders in the extrapyrimidal system result in?

A
  • Muscular rigidity
  • Tremors
  • Un-coordinated and abnormal muscle movements
  • Disturbances of postural reflexes
87
Q

What is parkinsons disease?

A

degenerative disease of basal ganglia

88
Q

What are the 6 clinical presentations of Parkinsons disease?

A
  • Hypokinesia (muscle rigidity & tremor at rest)
  • Mask-like expressionless face (drooling due to change of muscle tone and reflexes)
  • ‘pill-rolling’ tremor of hands
  • Bent posture (‘chasing’ centre of gravity)
  • Stiff shuffling gait
  • Difficulty initiating & controlling movements
89
Q

What are the causes of Parkinson’s disease?

A
  • Often Idiopathic (arising from unknown cause)
  • Sometimes follows stroke, viral infection & can be drug induced
90
Q

Which neurotransmitter loss is associated with parkinsons disease?

A

Dopamine from the basal ganglia

91
Q

How do drugs targetting parkinsons disease work?

A

Counteract the deficiency of dopmine in basal ganglia

OR

blocking muscarinic receptors

92
Q

How does the mid-brain present differently in parkinsons disease?

A

Pale substantia nigra due to reduced dopamine level

93
Q

What is the name of the neurotoxin precursor that causes the permanent symptoms of parkinsons disease?

A

MPTP (contminant of Meperidine) = destroys dopaminerginc neurones

94
Q

What are the two actions of dopamine in the body?

A

A neurotransmitter

Precursor for Noradrenaline!

95
Q

Which enzyme is responsible for converting dopamine into noradrenaline?

And where is this NOT found?

A

Beta-hydroxylase

Dopaminergic neurones

96
Q

How do we tell if dopaminergic neurones are present?

A

Detect the metabolic products of dopamine (DOPAC, HVA & sulphate conjugates) in urine = present

97
Q

Which enzyme degrades dopamine?

A

Monoamine oxidase B (MOA-B)

98
Q

Name a drug used to treat parkinsons disease that replaces dopamine:

Which two other drugs is this usually given in combination with?

A

Levodopa, Carbidopa & Entacopone

99
Q

Name 3 drugs used to treat parkinsons disease that mimic the action of dopamine:

A

Paramipexole

Ropinirole

Bromocriptine

100
Q

Name a drug used to treat parkinsons disease that causes the release of dopamine:

A

Amantidine

101
Q

Name two drugs used to treat parkinsons disease that act as MAO-B (monoaine oxidase beta) inhibitors:

A

Selegiline

Rasegiline

102
Q

Name a drug used to treat parkinsons disease that acts as an acetylcholine antagonist:

A

Benzatropine

103
Q

What is huntingtons disease? What causes it?

A

Neurodegenerative disease of the caudate nucleus

(atrophy = increased size of lateral ventricles & gliosis)= reduced acetylcholine and GABA in the striatumIt is a autosomal dominant genetic disorder

104
Q

What is gliosis?

A

Reactive change of glial cells in response to CNS damage= proliferation & hypertrophy of several different types of glial cells

105
Q

What are the 2 clinical features of huntingtons?

A
  • Abnormal choreiform movements (added movements outside of voluntary control)
  • Struggle to stop movement - Dementia (onset middle life)
106
Q

Which neurotransmitters go wrong in huntingtons disease?

A

Reduced acetylcholine & GABA in the striatum= hyperactivity of Dopaminergic synapses

107
Q

How do we treat huntingtons disease?

A

We treat the physiological issues e.g. decrease muscle tone

108
Q

Define dementia:

A

A structurally caused permanent or progressive decline in several dimensions of intellectual function that interferes substantially with the person’s normal sca; pr economical activity

109
Q

What are the two classifications of dementia?

A

Static dementia (fixed degree)

Progressive dementia (can accompany several major brain disorders)

110
Q

What causes dementia?

A

Static

Following a single major injury

Progressive

Primary cerebral cortical degeneration (Alzheimers)

Cerebrovascular disease (Multi infarct dementia)

Primary subcortial degeneration (Parkinsons)

Cerebral infections and inflammation (AIDs)

Prion diseases (CJD)

Toxic and metabolic (alcohol & hypothyroidism)

Tumours and hydrocephalus

Brain injury (subdural haematoma)

111
Q

At which age is prevalence of dementia highest?

A

>80 years old

112
Q

What is mental retardation?

A

Common insults that can occur to the developing brain and their consequences

113
Q

What is alzheimers disease?

A

Loss of cognitive function

Neurodegeneration of choliginergic neurons and other neurotransmitter systems (NA, 5-HT & Glu) -> mainly cortical areas

114
Q

What are the 3 histological features of azheimers?

(the only way you can 100% diagnose)

A
  • general brain atrophy (brain weight reduced by 30-40%!
    also: wider sulci, narrowed gyri mostly over frontal and parietal regions and larger ventricles due to loss of brain tissue)
  • extracellular plaques (Beta amyloid)
  • Intracellular tangles (tau proteins inside the neurones)
115
Q

What are the 4 mild symptoms of alzheimers?

A
  • confusion and memore loss (losing things & forgetting appointments)
  • Disorientation (getting lost in familiar surroundings)
  • Problems with routine tasks (e.g. unable to sort out finances)
  • changes in personality and judgement
116
Q

What are the 5 moderate symptoms of alzheimers?

A
  • difficulty with activities of daily living (feeding and bathing)
  • Anxiety, depression, paranoia, aggression, agitation, halucinations
  • Sleep disturbances
  • wandering/pacing
  • Difficulty recognising family and friends
117
Q

What are the 7 severe symtpoms of alzheimers?

A
  • Aphasia (problems understanding language)
  • Apraxia (inability to carry out tasks)
  • Agnosia (inability to recognise things)
  • Loss of speech- Loss of apetite (weight loss)
  • Loss of bladder and bowel control
  • Total dependence on caregiver (against infection pneumonia and stroke etc.)
118
Q

Which 3 enzymes are involved in the cleavage of amyloid precursor protein (APP) to produce amyloid protein (AP)?

Why is the balance between these three enzymes important?

A

Secretases alpha, beta and gamma

imbalance may be involved in amyloidgenesis

119
Q

Can amyloid protein aggregants be dissolved?

120
Q

What can be used as a good indicator of alzheimers?

A

The ApoE4 mutation

BUT

Some people with the mutation will not get alzheimers

121
Q

What are the two proposed theories of amyloid and neuronal death?

A

The amyloid may cause the death of the neurones

The death of neaurones may lead to amyloid developing

122
Q

Which two features of alzheimers are neurotoxic?

A

Amyloid plaques

Neurofibrillary tangles

123
Q

How do amyloid plaques affect neurones?

A

They block the network so there is imparired neuronal communication

124
Q

Following neuronal death in alzheimers what intracellular events occur that cause damage to the brain tissue?

A

Macrophages & the body responds to try and destroy the plaques -> body releases free radicals and enzymes into the area = goes into overdrive & releases cytokines etc. that damage the healthy neurones nearby

125
Q

How can some neurotransmitters cause damage to nearby neurones?

A

Exitotoxicity

126
Q

What causes alzheimers disease?

A

We don’t know!

Some theories:

  • APP mutations around beta and gamma secretase sites- Inherited defective gene
  • Aluminium intoxication = trace amount -> amyloid has metal binding area = possible shape change
127
Q

What are the 2 known risk factors of Alzheimers disease?

A

Age

Family history/genetic predisposition

128
Q

What are the 4 possible risk factors of alzheimers disease?

A

Head injury

Gender (women may have higher risk)

Educational levels (more years of formal education = less likely to develop)

Diet/lifestyle (high calorie, high fat, cholestrol & lack of excersize)

129
Q

What are the two types of licensed pharmacological therapy for alzheimers disease currently?

A
  • Cholinesterase inhibitors (increase ACh levels)
  • Partial NMDA (Ca influx) receptor antagonist = neuroprotective
130
Q

List 3 cholinesterase inhibitors:

A

Donepezil

Galantamine

Rivastigmine

131
Q

What are the side effects of cholinesterase inhibitors?

A

Abdominal pain

Nausea

Diarrhoea

132
Q

Name a partial NMDA receptor antagonist:

133
Q

What is CJD (creutzfeld-jacob disease)?

A

Neurodegenerative prion disease

134
Q

What is the adverage length of survival for CJD?

A

6 months

BUT

very long incubation period - could take a decade or longer!

135
Q

What are the two key clinical expressions of CJD?

A
  • Rapidly progressive dementia
  • Loss of motor co-ordination
136
Q

What causes CJD?

A

Prion infection (eating/close contact with BSE infected beef)- brain accumulates abnormal form (PrPsc) of the norally expressed prion protein (PrPc) -> evidence PrPsc is infective agent (not DNA or RNA & = v. resistant)

137
Q

List some expermimental drugs being used to inhibit aggregation of PrPsc protein;

A

Quinacrine (antimalarial)

Chlorpromazine (antipsyhchotic)

Pentosan polyphospate (glycosidic polymer)

138
Q

What is multiple sclerosis?

A

A slowly progressive autoimmune CNS disease characterised by disseminated patches of demyelination (damaged glial cells = oligodendrocytes) in the brain and sinal cord = multiple and varies neurological symptoms and signs usually with remissions and exacerbations

139
Q

What is the age of onset for Multiple sclerosis?

A

20-45 years

140
Q

What is a risk factor for multiple sclerosis?

A

Vitamin D deficiency (risk higher away from equator)

141
Q

What is the importance on where you live and your susceptibility to multiple sclerosis?

A

Susceptibility is set by where you lived for the first 8 years of your life

142
Q

Where do the problems in multiple scelrosis stem from?

A

Miscommunication in remyelination pathways e.g. osteocytes invade = cytokine release = glial progenitor cells cannot infiltrate = no repair & cell death

143
Q

Which cells cause remyelination (repair glial cells)?

A

Glial progenitor cells

144
Q

What are the 4 methods of treatment for multiple scleorsis?

A
  • minimization of handicap (physio, occupational therapy & adaptions to work and home environments)
  • Suppress inflammation during acute relapse
  • Reduce relapse rates and suppress ongoing disease activity
  • Control of muscle tone
145
Q

Which drug is used to treat Multiple scleoris through suppressing inflammation during acute relapse?

A

Methylprednisolone (corticosteroids -> N.B. no effect on long term outcome)

146
Q

Which 4 drugs are used to treat multiple scleoris through reducing relapsse rates and suppressing ongoing disease activity?

A

Interferon Beta (may also reduce the rate at which patients progress from a single episode of CNS demyleination progresses to MS)

Glatiramer acetate

Natalizumab

Azothiopine (intravenous IgG)

147
Q

Which 5 drugs are used to treat multiple sclerosis by controlling muscle tone?

A

Baclofen

Benzodiazepines

Tizadine

Botulinum toxin

Dantrolene

148
Q

List 3 anti-obesity drugs that work in the CNS:

A

Sibutramine

Phentermine

Fenfluramine

149
Q

What is sibutramine?

A

A noradrenaline/ serotonin (5-HT) reuptake inhibitor

150
Q

What is phentermine?

A

A sympathomimetic

151
Q

What is fenfluramine?

A

A serotonin (5-HT) reuptake inhbitor

152
Q

Which drug is used for anorexia and bulimia?

A

Fluoxetine (Prozac)

153
Q

What is fluoxetine?

A

A selective serotonin reuptake inhibitor

154
Q

Which other receptor is the target of atypical antipsychotics?

and are these drugs agonists or antagonists of this type of receptor?

A

5-HT2 antagonism

155
Q

What is the mode of action for most antidepressants and antipsychotics?

A

NA or serotonin reuptake inhibiors

156
Q

What is depression?

A

A unipolar mood disorder that makes the individual feel down

157
Q

What is mania?

A

A unipolar mood disorder that is bad for the patients environment (over-excited) = inappropriate behaviour

158
Q

What is manic depression?

A

A bipolar mood disorder causing the individual to fluctuate between feeling down and being over-excited

159
Q

What are the three different causes of mood disorders?

A

Reactive (response to traumatic life events)

Endogenous (no obvious cause)

Side effect of drug treatment (e.g. rimonabant =put on weight & interferon alpha = hepatitis c or interfering with alzheimers treatment)

160
Q

How long does it take for antidepressants and antipshycotics to start working?

A
  • 6-8 weeks (levels increse gradually & stays in system for several weeks after stop taking)

N.B. cannot just cut off drug as body starts to rely on drug so doesnt function properly without it

161
Q

What are the 5 main symptoms of mania?

A
  • sleep changes (need less)
  • Excessive exuberance, enthusiasm, confidence and grandiosity
  • increased libido
  • behaviours inappropriate to circumstances
  • Disorders of thought (psychosis)
162
Q

What are the 5 things thought to cause depression?

A

Chemical imbalance (monoamine theory of depression, functional serotonin/NA/DA deficit)

Neurodegeneration (neuronal apoptosis and neurogenesis)

Immune response (sickness behaviour)

Genes

Environment (stress)

163
Q

What are the 3 types of treatments for the depressed?

A

Pharmacological (enhance monoamine levels in CNS & specific receptor agonists/antagonists)

Cognitive behavioural therapy

Neurological interventions (electroconvulsive shock therapy, deep brain stimulation, vagal nerve stimulation)

164
Q

In which two ways can monoamine levels in the CNS be enhanced?

A

Monoamine re-uptake inhibitors

Monoamine oxidase inhibitors receptor antagonists

165
Q

Name a post-synaptic receptor agonist that increases monoamine function in the CNS:

166
Q

Name a pre-synaptic receptor antagonist that increases monoamine function in the CNS:

A

Mirtazapine

167
Q

Name four mono-amine oxidase enzyme inhibitors:

Which is reversible and which is irreversible?

A

Moclobemide (reversible)

Phenylzine (irreversible)

Iproniazid

Tranylcypromine

168
Q

State the key things about Monoamie oxidases and how they work:

A

Inhibits breakdown of monoamines

Inhibit monoamine oxidase A or B -> (MAOA prefers 5HT & MAOB prefers DA & NA)

Both reversible and irreversible MOA found in all tissues including GI tract Multiple side effects -> M1, alpha 2, H1. 5-HT2, cheese reaction & drug interactions

169
Q

Name two monoamine reuptake inhibitors:

A

Fluoxetine

Venlafaxine

170
Q

What are the two different classes of antidepressants?

A

Typical=

Tricyclic antidepressants (TCAs) & specific reuptake inhibitors

Atypical

= mixed uptake blockers and receptor blocking drugs

171
Q

What is similar between the two classes?

A

similar efficacy

delayed onset despite different modes of action

172
Q

TYPICALName 4 tricyclic antidepressants:

A

Imapramine

Amitriptyline

Clominpramine

Desipramine

173
Q

What are the two mechanism of action of tricyclin antidepressants?

A

Block NA &/or 5-HT reuptake (relative selectivity varies)

Some block alpha 2 adrenoreceptors

Many have active metabolites (long lasting effect)

174
Q

What is the main side effect of Tricyclic antidepressants (TCA’s)?

A

Cardiotoxicity = low theraputic index and cause tachycardia, arrythmias & hypotension

N.B. there are many side effects

175
Q

TYPICALName 3 Selective Serotonin reuptake inhibitors (SSRI’s)

A

Fluoxetine

Paroxetine

Citalopram

176
Q

Which 5 side effect improvements of SSRIs make it preferable to TCAs?

A

Lack of cholinergic side effects

Less weight gain

Low toxicity in overdose

No food interaction

Reduced drug interaction

177
Q

What are the 5 5-HT related side effects of SSRI’s?

A

Nausea (5-HT3)

Anorexia (5-HT2)

Insomnia (5-HT2)

Sexual dysfunction (5-HT2)

5-HT syndrome = similar to ecstacy overdose

178
Q

TYPICALName 1 Selective noradrenalne reuptake inhibitor (NARI)

A

Reboxetine

179
Q

ATYPICALName 1 serotonin-noradrenaline reuptake inhibitor (SNRI)

A

Venlafaxine = used in severly depressed, retarded, hypersomnic, weight gaining, atypical depressives

180
Q

ATYPICAL Name 1 5-HT2 antagonist + SSRI

181
Q

ATYPICALName 1 5-HT2 antagonist + SNRI/SSRI

A

Nefazedone= reduced anxiety, imporved slow wave sleep, reduce sexual dysfunction & sedation

182
Q

ATYPICALName two alpha 2 adrenoreceptor and 5-HT antagonist

A

Mianserin

Mirtazapine= increased NA & 5-HT by blockade of pre-synaptic inhibition

5-HT antagonist = reduces side effect

183
Q

Which two drugs/chemicals are used as mood stabilsiers to control mania?

A

Lithium -> mechanism poorly understood (interacts with g proteins & inhibit ability to transduce signal or alter enzynes that interact with second messanger systems):(

Caution: potential toxicicity = careful monitering

Anti-epileptic drugs:

Valproic Acid - inhibits GABA transaminase = some effect on Na channelsCarbamazepine - use dependent block of Na channelsOlanzapine- Atypical antipsychotic

184
Q

What is the treatment for mild/moderate depression?

A

Cognitive therapy

185
Q

What is the treatment for sever depression?

186
Q

What is the treatment for very severe/drug resistant depression?

A

Elektroconvulsive therapy & deep brain stimulation (dual or triple therapy)

187
Q

What are the first line drugs used for depression?

A

SSRI (selective seretoning reuptake inhibitors)

188
Q

What are the second line drugs for depression?

A

Monoamine oxidase inhbitors

189
Q

After remission from depression a patient should continue taking antidepressants for how long?

A

6-12 months

190
Q

What are the 6 other applications for reuptake inhibitors?

A

Obsessive compulsive disorders

Panic disorder

Social phobia

Anxiety disorders

Eating disorders (bulimia/ binge eating)

Obesity

191
Q

What are the two other applications for tricylic antidepressants (TCAs)?

A

Novel analgesic agent (amitryptyline)

Migraine prophylaxis drug (amitryptyline)

192
Q

What are the two major classes of antipsychotic (neuroleptic) drugs = control behavioural disorders such as schizophrenia?

which receptors do they act at?

A

Typical anti-psychotic drugs = D2 receptor antagonists (with multiple sites of action)

Atypical anti-psychotic drugs = serotonin and dopamine antagonists

193
Q

List the two types of typical antipshycotic drugs:

A

Phenothiazines (chlorpramazine)Biturophenones (haloperidol)

194
Q

Name 3 Atypical antipsychotic drugs:

A

Clozapine

Risperidone

Aripriprazole

195
Q

The distinction between typical and atypical antipsychotics depends on which 4 properties?

A

Receptor profile incidence of extrapyrimidal side effects (fewer in atypical) efficacy in treatment-resistace group of patients (especially clozapine) efficacy against negative symptoms

196
Q

What is the aim of mixed D2 and 5-HT2 antagonists?

A

Reduce motor side effects and improve treatment of negative symptoms 5-HT2 antagonism = reduced overall D2 blockade through 5-HT DA interactions (reduced extrapyrimidal, hormonal and cognitive side effects)

D2 antagonist = retain sufficient block to counter psychotic symptoms

197
Q

What are the 6 side effects of 5HT2-DA2 receptor antagonists?

A

Endocrine (hyperprolactinaemia)

Anti-muscarinic (urinary retention, dry mouth & blurred vision) Anti alpha adrenoreceptor (hypotension)

Anti-histamine H1 (sedation)

5-HT2 (weight gain)

Idiosyncratic/Hypersensitivity reactions

198
Q

why are typical drugs not used so much any more?

A

Ineffective at relieving negative symptoms

199
Q

Which 3 drugs are the first line of treatment in schizophrenia?

A

Quetapine

Zotepine

Risperidone= ATYPICAL ANTI-PSYCHOTIC DRUGS

200
Q

What is the name of the second line drug?

And which risk is associated with it?

A

Clozapine (ATYPICAL)

Risk of agranulocytosis

201
Q

Which drug is widely used in severe psychotic patients?

A

Haloperidol (TYPICAL ANTI-PSYCHOTIC)

202
Q

What is the other application for typical antipsychotic drugs?

203
Q

What are the three other applications for atypical antipsychotic drugs?

A

Conduct disorders

ADHD non-responders

Behavioural symptoms of alzheimers disease

Yr 2 - Pharmacology (18 decks)

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